I am starting this thread to demystify the most feared subject among medical students and general practitioners alike. Many a times the neuro part of the examination is very superficial and does not yield anything. I will touch upon many such areas in this thread. I will make sure that it's high value and everybody who visits this thread finds something interesting and beneficial. Any member who wishes to contribute with clinical points are welcome. please refrain from posting any praises or thank you messages. not my intention of starting this thread...as this takes a lot of reading and then a big heart to dish it out on a plate - so, encouragement and appreciation are welcome. But please do that by either pushing the thanks button, or the like button or giving rep points (-:
'Triple H' in the context of SAH One complication of aneurysmal subarachnoid hemorrhage is the development of vasospasm. Approximately 1 to 2 weeks following the initial hemorrhage, patients may experience 'spasm' of the cerebral arteries, which can result in stroke. The etiology of vasospasm is thought to be secondary to an inflammatory process that occurs as the blood in the subarachnoid space is resorbed. It appears that macrophages and neutrophils that enter the subarachnoid space to phagocytose senescent erythrocytes and clear extracorpuscular hemoglobin, remain trapped in the subarachnoid space, die and degranulate 3”“4 days after their arrival, and release massive quantities of endothelins and free radicals that in turn induce vasospasm. Vascular narrowing, however, is only one component of the transient inflammatory injury, which is extensive. Vasospasm is monitored in a variety of ways. Non-invasive methods include transcranial Doppler, which is a method of measuring the velocity of blood in the cerebral arteries using ultrasound. As the vessels narrow due to vasospasm, the velocity of blood increases. It is possible to screen for the development of vasospasm with transcranial doppler every 24”“48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm The amount of blood reaching the brain can also be measured by CT or MRI or nuclear perfusion scanning. The definitive, but invasive method of detecting vasospasm is cerebral angiography. In order to prevent or reduce the risk of permanent neurological deficits, or even death, vasospasm should be treated aggressively. → This is usually performed by early delivery of drug and fluid therapy, or 'Triple H' (hypertensive-hypervolemic-hemodilution therapy) (which elevates blood pressure, increases blood volume, and thins the blood) to drive blood flow through and around blocked arteries. → For patients who are refractive (resistant) to Triple H therapy, narrowed arteries in the brain can be treated with medication delivered into the arteries that are in spasm and with balloon angioplasty to widen the arteries and increase blood flow to the brain. Although the effectiveness of these treatments is well established, angioplasty and other treatments delivered by interventional radiologists have been in evolution over the past several years. It is generally recommended that aneurysms be evaluated at specialty centers which provide both neurosurgical and interventional radiology treatment and which also permit angioplasty, if needed, without transfer. - Ref : Wiki - http://en.wikipedia.org/wiki/Subarachnoid_hemorrhage; Cerebral aneurysm - Wikipedia, the free encyclopedia Caution Please don’t get carried away by the hypertension component of Triple H therapy. That’s not our goal. Our goal is perfusion. So Nimodipine first and even if we have to infuse fluid (which will invariably raise the BP) to increase cerebral perfusion, it should be after the aneurysms have been taken care of by either clipping if in the MCA region (because the interventional radiologist can’t reach) or by coiling in the posterior circulation ( because the neurosurgeon can’t reach). ”˜Triple H’ is one of the classic scenarios of risk/reward trade-off in medicine. (-:
New Treatment for Tourettes Syndrome ( Must watch ) Many of you may already have known this, but it was new to me. Please note : This is for a subset of Tourettes...more in the video Code: http://www.youtube.com/watch?v=CpiGEO0ueME&feature=related (-:
40 yr old gorgeous woman walks into ur lavish neurology clinic A 40 yr old gorgeous woman walks into ur lavish neurology clinic (-:, complaining of rt. shoulder weakness and pain ): . One thing we will all do is establish a chronology...fine and +/- systems review. Then we will immediately proceed to a neuro exam ( in this case focused ) and pin the cause to a C5 radiculopathy..may ask for a Cervical Xray next and even if it shows something that is just a distant cousin of cervical spondylosis, then we will end our investigation there. What else could have been a possibility here - If she is gorgeous and well toned, then she must be into some kind of physical activity to stay that way at 40. She could well be having a SLAP or Bankart lesion of the shoulder from either weight training or overhead activities like tennis. An Obrein test or any of the several for anterior instability if combined with the neurological exam will help differentiate this primary msk problem from a perceived neuro problem ( the muscle weakness and pain in this case being secondary to disuse following shoulder injury....on the same lines as hand - shoulder syndrome following Colle's fracture.) It could be an endocrinopathy ex - hypothyroidism. Hypothyroidism doesn't care whether u r gorgeous, play sports, love children or say ur daily prayers esp. the autoimmune variety has a penchant for young gorgeous women. Less likely, but still needs to be ruled out are the autoimmune myopathies. Bottomline : When looking at a perceived neuro problem esp. peripheral, look at it thru the lens of an orthopedician, a rheumatologist and endocrinologist in addition to donning ur neuro hat. (-:
have come up with the above table after going through a number of standard resources and as you all know slight variation is expected from book to book. [TABLE="class: MsoTableGrid"] [TR] [TD="width: 155"] Nerve root [/TD] [TD="width: 282"] Reflex [/TD] [TD="width: 372"] Muscle axn [/TD] [TD="width: 270"] Sensory distribution [/TD] [/TR] [TR] [TD="width: 155"] C5 [/TD] [TD="width: 282"] biceps [/TD] [TD="width: 372"] deltoid, biceps [/TD] [TD="width: 270"] lateral arm [/TD] [/TR] [TR] [TD="width: 155"] C6 [/TD] [TD="width: 282"] brachioradialis [/TD] [TD="width: 372"] wrist extension [/TD] [TD="width: 270"] lateral forearm & palmar thumb [/TD] [/TR] [TR] [TD="width: 155"] C7 [/TD] [TD="width: 282"] triceps [/TD] [TD="width: 372"] triceps, finger extension [/TD] [TD="width: 270"] long finger [/TD] [/TR] [TR] [TD="width: 155"] C8 [/TD] [TD="width: 282"] none [/TD] [TD="width: 372"] finger flexion [/TD] [TD="width: 270"] medial forearm & little finger [/TD] [/TR] [TR] [TD="width: 155"] L4 [/TD] [TD="width: 282"] knee jerk [/TD] [TD="width: 372"] knee extension, ankle dorsiflexion [/TD] [TD="width: 270"] medial leg and ankle [/TD] [/TR] [TR] [TD="width: 155"] L5 [/TD] [TD="width: 282"] post. tibial tendon (20% popul[SUP]n[/SUP]) [/TD] [TD="width: 372"] extensor hallux longus (other extensors also) [/TD] [TD="width: 270"] lateral calf and dorsal foot [/TD] [/TR] [TR] [TD="width: 155"] S1 [/TD] [TD="width: 282"] Ankle jerk [/TD] [TD="width: 372"] plantar flexion (toe and ankle flexors), foot eversion [/TD] [TD="width: 270"] posterior calf, lateral border of foot and sole [/TD] [/TR] [TR] [TD="width: 155"] Myelopathy (similar to UMN ”“ below level of lesion and LMN ”“ at lvel of lesion)) [/TD] [TD="width: 282"] Hyperreflexia with clonus, + Babinski or Hoffman sign [/TD] [TD="width: 372"] Diffuse weakness, increased muscle tone,rigidity [/TD] [TD="width: 270"] Diffuse hyperesthesias [/TD] [/TR] [/TABLE] (-:
Important dermatomes and anatomical landmarks Following is a list of spinal nerves and points that are characteristically belonging to the dermatome of each nerve: C2 - At least one cm lateral to the occipital protuberance at the base of the skull. Alternately, a point at least 3 cm behind the ear. C3 - In the supraclavicular fossa, at the midclavicular line. C4 - Over the acromioclavicular joint. C5 - On the lateral (radial) side of the antecubital fossa, just proximally to the elbow. C6 - On the dorsal surface of the proximal phalanx of the thumb. C7 - On the dorsal surface of the proximal phalanx of the middle finger. C8 - On the dorsal surface of the proximal phalanx of the little finger. T1 - On the medial (ulnar) side of the antecubital fossa, just proximally to the medial epicondyle of the humerus. T2 - At the apex of the axilla. T3 - Intersection of the midclavicular line and the third intercostal space T4 - Intersection of the midclavicular line and the fourth intercostal space, located at the level of the nipples. T5 - Intersection of the midclavicular line and the fifth intercostal space, horizontally located midway between the level of the nipples and the level of the xiphoid process. T6 - Intersection of the midclavicular line and the horizonal level of the xiphoid process. T7 - Intersection of the midclavicular line and the horizontal level at one quarter the distance between the level of the xiphoid process and the level of the umbilicus. T8 - Intersection of the midclavicular line and the horizontal level at one half the distance between the level of the xiphoid process and the level of the umbilicus. T9 - Intersection of the midclavicular line and the horizontal level at three quarters of the distance between the level of the xiphoid process and the level of the umbilicus. T10 - Intersection of the midclavicular line, at the horizontal level of the umbilicus. T11 - Intersection of the midclavicular line, at the horizontal level midway between the level of the umbilicus and the inguinal ligament. T12 - Intersection of the midclavicular line and the midpoint of the inguinal ligament. L1 - Midway between the key sensory points for T12 and L2. L2 - On the anterior medial thigh, at the midpoint of a line connecting the midpoint of the inguinal ligament and the medial epicondyle of the femur. L3 - At the medial epicondyle of the femur. L4 - Over the medial malleolus. L5 - On the dorsum of the foot at the third metatarsophalangeal joint. S1 - On the lateral aspect of the calcaneus. S2 - At the midpoint of the popliteal fossa. S3 - Over the tuberosity of the ischium or infragluteal fold S4 and S5 - In the perianal area, less than one cm lateral to the mucocutaneous zone SOURCE - Wiki (-:
Imp. Points to remember while intepreting the lumbar puncture results for SAH Imp. Points to remember while intepreting the lumbar puncture results for SAH Lumbar puncture will show evidence of hemorrhage in 3% of people in whom CT was found normal; lumbar puncture is therefore regarded as mandatory in people with suspected SAH if imaging is negative. At least three tubes of CSF are collected. If an elevated number of red blood cells is present equally in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that it is due to damage to a small blood vessel during the procedure (known as a "traumatic tap"). While there is no official cutoff for red blood cells in the CSF no documented cases have occurred at less than "a few hundred cells" per high-powered field. The CSF sample is also examined for xanthochromia—the yellow appearance of centrifugated fluid. More sensitive is spectrophotometry (measuring the absorption of particular wavelengths of light) for detection of bilirubin, a breakdown product of hemoglobin from red blood cells. Xanthochromia and spectrophotometry remain reliable ways to detect SAH several days after the onset of headache. An interval of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the hemoglobin from the red blood cells to be metabolized into bilirubin. Ref – Wiki - Subarachnoid hemorrhage - Wikipedia, the free encyclopedia (-:
A classic case to differentiate peripheral from central vertigo A classic case to differentiate peripheral from central vertigo [FONT=&]A 27-year-old patient with a chief complaint of mild vertigo of 3-months duration is seen by a neurologist. Examination reveals a positional (horizontal and vertical) nystagmus that is bidirectional. The patient reports the absence of tinnitus. Which of the following is the most likely etiology of the vertigo?[/FONT] [FONT=&]A. Labyrinthitis[/FONT] [FONT=&]B. Ménière's syndrome[/FONT] [FONT=&]C. Lesion of the flocculonodular lobe of the cerebellum[/FONT] [FONT=&]D. Lesion of the spinocerebellum[/FONT] [FONT=&]E. Psychogenic[/FONT] [FONT=&]EXPLANATION: Pathologic vertigo is generally classified as peripheral (labyrinthine) or central (brainstem or cerebellum). The clinical presentation in this case is most consistent with central vertigo. Positional (especially horizontal) nystagmus (to-and-fro oscillation of the eyes) is common in vertigo of central origin, but absent or uncommon in peripheral vertigo. The chronicity of the vertigo is characteristic of central vertigo, whereas the symptoms of peripheral vertigo generally have a finite duration and may be recurring. Tinnitus and/or deafness is often present in peripheral vertigo, but absent in central vertigo. The flocculonodular lobe, or vestibulocerebellum, is connected to the vestibular nuclei and participates in the control of balance and eye movements, particularly changes in the vestibuloocular reflex (VOR), which serves to maintain visual stability during head movement; a lesion of this area of the cerebellum may result in vertigo and nystagmus, whereas the spinocerebellum is involved in the coordination of limb movement. Labyrinthitis and Ménière's syndrome are examples of vertigo of peripheral origin. In psychogenic versus organic vertigo, nystagmus is absent during a vertiginous episode.[/FONT] [FONT=&]The answer is C.[/FONT] (-:
A classic case to remember structures passing thru Sup. orbital fissure A classic case to remember structures passing thru Sup. orbital fissure often get quized on the exam regarding structures passing thru sup. orbital fissure. the case below shud help (-:
Lesion in rostral vs Caudal medulla The following are 2 classic cases to differentiate a lesion in the rostral vs caudal ventro-medial medulla. [FONT=&]A 65-year-old male with a history of heart disease is admitted to the emergency room after having been found unconscious in his home. When the patient regains consciousness and is examined by a neurologist, it was discovered that he cannot identify the presence of a tuning fork, pencil, or pressure applied to his left leg. In addition, the patient is unable to move his left leg or arm. Other clinical signs are not apparent. Which of the following regions most likely accounts for the deficits described?[/FONT] [FONT=&]A. Ventromedial aspect of medulla-spinal cord border[/FONT] [FONT=&]B. Rostral aspect of the ventromedial medulla[/FONT] [FONT=&]C. Dorsolateral aspect of the caudal aspect of medulla[/FONT] [FONT=&]D. Dorsomedial aspect of the pontine tegmentum[/FONT] [FONT=&]E. Dorsomedial aspect of the midbrain tegmentum[/FONT] [FONT=&]EXPLANATION: In this case, there were no dysfunctions reported concerning his ability to move his tongue and there were no speech deficits. This indicates that the lesion could not have been at the level of the caudal ventromedial medulla, (especially since the medial lemniscus is not present at this level and the dorsal columns are located in a dorsal position), but rather at a somewhat more rostral level of the ventromedial medulla, which includes the pyramidal tract and medial lemniscus, but not the hypoglossal nucleus and nerve. The other choices do not include pyramids or medial lemniscus. [/FONT] [FONT=&]The answer is B.[/FONT] Moral of story - If u loss of post column function + umn motor weakness on the same side - lesion is in rostral ventromedial medulla xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx A case of lesion in caudal ventro-medial medulla b4 pyramidal decussation [FONT=&]A patient displays a deviation of the tongue to the left and a hemiparesis on the right side. The lesion is located in which of the following regions?[/FONT] [FONT=&]A. Right hypoglossal nucleus[/FONT] [FONT=&]B. Left hypoglossal nucleus[/FONT] [FONT=&]C. Right inferior frontal lobe[/FONT] [FONT=&]D. Right ventromedial medulla[/FONT] [FONT=&]E. Left ventromedial medulla [/FONT] [FONT=&]EXPLANATION: A lesion of the left ventromedial medulla would produce a disorder referred to as "alternating hypoglossal hemiplegia" in which there is damage to the hypoglossal nerve as it is about to exit the brainstem and to the pyramidal tract. Damage to the hypoglossal nerve causes a deviation of the tongue to the side of the lesion when it is protruded and a contralateral UMN paralysis of the limbs because these descending corticospinal fibers cross at the medulla-spinal cord border. The other choices do not include structures that were affected in this case. The choice involving the right ventromedial medulla is incorrect because the tongue deviated to the left, not the right side and the paralysis was on the right side of the body, not the left.[/FONT] [FONT=&]The answer is E. [/FONT]
Greater( Superficial ) Petrosal vs Deep petrosal vs Lesser petrosal nerve Greater( Superficial ) Petrosal vs Deep petrosal vs Lesser petrosal nerve Many a times we get confused with these 3 structures and hence I am putting them all together one below the other. The greater (superficial) petrosal nerve is a branch of the facial nerve that arises from the geniculate ganglion, a part of the facial nerve inside the facial canal. It enters the middle cranial fossa through the greater (superficial) petrosal foramen (on the anterior surface of the petrous temporal bone). It proceeds towards the foramen lacerum, where it joins the deep petrosal nerve (sympathetic) to form the nerve of the pterygoid canal (vidian nerve ). The nerve of the pterygoid canal passes through the pterygoid canal to reach the pterygopalatine ganglion. Function The greater (superficial) petrosal nerve carries gustatory (taste) and parasympathetic fibres. Postganglionic parasympathetic fibres from pterygopalatine ganglion supply lacrimal gland and the mucosal glands of the nose, palate, and pharynx. The gustatory fibres do not relay in the ganglion and are distributed to the palate. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx The deep petrosal nerve (large deep petrosal nerve) is given off from the carotid plexus, and runs through the carotid canal lateral to the internal carotid artery. It then enters the cartilaginous substance which fills the foramen lacerum, and joins with the greater superficial petrosal nerve to form the nerve of the pterygoid canal, also known as the Vidian nerve. Function It carries postsynaptic sympathetic nerve fibers to the pterygopalatine ganglion, also known as the sphenopalatine ganglion.These fibers innervate blood vessels and mucous glands of the head and neck. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx The lesser petrosal nerve consists of parasympathetic fibres. It exits the jugular foramen with the glossopharyngeal nerve, only to reenter the skull through the tympanic canaliculus. It then leaves the tympanic plexus to exit through the hiatus for lesser petrosal nerve and finally exits through the skull through the foramen ovale, synapsing in the otic ganglion. Post-synaptic parasympathetic fibers then provide innervation to the parotid gland (by hitchhiking) with the auriculotemporal nerve (from V3). then who the fu.. is the tympanic verve ???????????????? The tympanic nerve (nerve of Jacobson) is a branch of the glossopharyngeal nerve found near the ear. Path It arises from the petrous ganglion, and ascends to the tympanic cavity through a small canal, the fossula petrosa/tympanic canaliculus, on the under surface of the petrous portion of the temporal bone on the ridge which separates the carotid canal from the jugular fossa. In the tympanic cavity it divides into branches which form the tympanic plexus and are contained in grooves upon the surface of the promontory. Jacobson's nerve contains both sensory and secretory fibers. Sensory fibers supply the middle ear. Parasympathetic secretory fibers continue as the Lesser Petrosal nerve and provide secretomotor innervation to the parotid gland. The secretory fibers enter the otic ganglion. The postganglionic parasympathetic fibers are then distributed via the auriculotemporal nerve (branch of the trigeminal nerve) to the parotid gland. Sympathetic fibers (for the large deep petrosal nerve) through communication with the carotid plexus. Clinical significance This nerve may be involved by paraganglioma, in this location referred to as glomus jugulare or glomus tympanicum tumours. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx We also need to know a little bit about the auriculotemporal nerve in connection with the lesser petrosal nerve. The auriculotemporal nerve is a branch of the mandibular nerve that runs with the superficial temporal artery and vein, and provides sensory innervation to various regions on the side of the head. Origin The auriculotemporal nerve arises as two roots from the posterior division of the mandibular nerve and encircle the middle meningeal artery (a branch of the mandibular part of the maxillary artery, which is in turn a terminal branch of the external carotid artery). The roots then converge to form a single nerve. Course The auriculotemporal nerve passes medially to the neck of the mandible, gives off parotid branches and then turns superiorly, posterior to its head and moving anteriorly, gives off anterior branches to the auricle. It then crosses over the root of the zygomatic process of the temporal bone, deep to the superficial temporal artery. Innervation The somatosensory root (superior) originates from branches of the mandibular nerve, which pass through the otic ganglion without synapsing. Then they form the somatosensory (superior) root of the auriculotemporal nerve. The two roots re-unite and shortly after the branching of secretomotor fibers to the parotid gland (parotid branches) the auriculotemporal nerve comprises exclusively somatosensory fibers, which ascend to the superficial temporal region. There, it supplies the auricle, external acoustic meatus, outer side of the tympanic membrane and the skin in the temporal region (superficial temporal branches). It also carries a few articular branches which go on to supply the temporomandibular joint. The parasympathetic root (inferior) carries postganglionic fibers to the parotid gland. These parasympathetic, preganglionic secretomotor fibers originate from the glossopharyngeal nerve (CN IX) as one of its branches, the lesser petrosal nerve. This nerve synapses in the otic ganglion and its postganglionic fibers form the inferior, parasympathetic root of the auriculotemporal nerve. The two roots re-unite and shortly after the "united" auriculotemporal branch gives off parotid branches, which serve as secretomotor fibers for the parotid gland. Clinical significance This nerve as it courses posteriorly to the condylar head, is frequently injured in temporomandibular joint (TMJ) surgery, causing an ipsilateral parasthesia of the auricle and skin surrounding the ear. Actually, it is the main nerve that supplies the TMJ, along with branches of the masseteric nerve and the deep temporal. After a parotidectomy, the nerves from the Auriculotemporal Nerve that previously innervated the parotid gland can reattach to the sweat glands in the same region. The result is sweating along the cheek with the consumption of foods (Frey's syndrome). Treatment involves the application of an antiperspirant or glycopyrrolate to the cheek, Jacobsen's neurectomy along the middle ear promontory, and lifting of the skin flap with the placement of a tissue barrier (harvested or cadaveric) to interrupt the misguided innervation of the sweat glands. Pain related to a condition called parotitis, a cause of which is "mumps", will be carried by the auriculotemporal nerve. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Source : The above material is from 5 diff. articles of Wiki. It was looking like a ruffled head and so i gave it a nice hair cut. It will still take some effort to get this down P:
Parasympathetic Ganglia of the head and neck Parasympathetic Ganglia of the Head and Neck Often a source of pain in the exams, becos most people skip and those who are brave enough to learn, may no remember it in the heat of the exam ( will b like ciliary ganglion....ciliary what ????????????? >?>?.. ) So I will be covering the 4 parasym. ganglia in the precise order of the cranial nerves that they relate to 1) The ciliary ganglion is a parasympathetic ganglion located in the posterior orbit. It measures 1”“2 millimeters in diameter and contains approximately 2,500 neurons.[SUP][/SUP] Preganglionic axons from the Edinger-Westphal nucleus travel along the oculomotor nerve and form synapses with these cells. The postganglionic axons run in the short ciliary nerves and innervate two eye muscles: the sphincter pupillae constricts the pupil, a movement known as Miosis. The opposite, Mydriasis, is the dilation of the pupil. the ciliaris muscle contracts, releasing tension on the Zonular Fibers, making the lens more convex, also known as accommodation. Three types of nerve fibers run through the ciliary ganglion: parasympathetic fibers, sympathetic fibers and sensory fibers. Only parasympathetic fibers form synapses in the ganglion. The other two types of nerve fibers simply pass through. In classical anatomy, the ciliary ganglion is said to have three “roots:” a parasympathetic root of ciliary ganglion (or motor root) a sympathetic root of ciliary ganglion a sensory root of ciliary ganglion [h=2]Diseases[/h] [h=3]Light-near dissociation[/h] In some neurological disorders, the pupil does not react to light, but it does react to accommodation. This is called “light-near dissociation”. In Adie syndrome, damage involving the ciliary ganglion manifests light-near dissociation and a tonically dilated pupil (usually unilateral). Other causes of light-near dissociation involve damage to the brainstem[SUP][/SUP], where a tonic pupil is not produced. Brainstem causes of light-near dissociation include Argyll Robertson pupil and Parinaud syndrome. Irene Loewenfeld is generally credited for being the first physiologist to make this distinction. [h=3]Adie tonic pupil[/h] Diseases of the ciliary ganglion produce a tonic pupil.[SUP][/SUP]This is a pupil that does not react to light (it is “fixed”) and has an abnormally slow and prolonged response to attempted near vision (accommodation). When a patient with an Adie pupil attempts to focus on a nearby object, the pupil (which would normally constrict rapidly) constricts slowly. On close inspection, the constricted pupil is not perfectly round. When the patient focuses on a more distant object (say the far side of the room), the pupil (which would normally dilate immediately) remains constricted for several minutes, and then slowly dilates back to the expected size. Tonic pupils are fairly common ”“ they are seen in roughly 1 out of every 500 people. A patient with anisocoria (one pupil bigger than the other) whose pupil does not react to light (does not constrict when exposed to bright light) most likely has Adie syndrome ”“ idiopathic degeneration of the ciliary ganglion. [h=4]Physiology[/h] The strange behavior of tonic pupils was first explained by Irene Loewenfeld in 1979. The ciliary ganglion contain many more nerve fibers directed to the ciliary muscle than nerve fibers directed to the constrictor pupillae ”“ roughly twenty times more. The ciliary muscle is also more massive than the constrictor pupillae, again by a factor of twenty. Based on these observations, Loewenfeld proposed an explanation of the tonic pupil. She noted that pathological destruction of nerve cells in the ciliary ganglion that is found in all cases of Adie pupil. In her own words[SUP][/SUP]: Let’s say that in a given fresh Adie’s pupil, a random 70% of the cells in the ciliary ganglion stop working; and that, in a couple of months, these neurons re-grow and randomly re-innervate both intraocular sphincters (the ciliary muscle and the iris sphincter). Some parasympathetic light-reaction neurons that were originally destined for the iris sphincter will end up innervating the ciliary muscle. But there will not be enough of them to budge that big muscle, so there will be no detectable accommodation with exposure to light. The other way around, it is a different story. There will be plenty of accommodative neurons re-growing into the iris sphincter, and it won’t take very many of them to make a little muscle like the iris sphincter contract. This means that every time the patient accommodates her gaze to a near object, some of the innervation to the ciliary muscle will spill over into the iris and constrict the pupil. Loewenfeld’s theory is now generally accepted. It explains the defining features of a tonic pupil: (1) The pupil does not react to light. The original light-reaction neurons have been destroyed. (2) Tonic constriction with attempted near vision. Aberrant regeneration of nerve fibers intended for the ciliary muscle causes abnormal, tonic contraction of the pupil with accommodation. (3) Segmental iris constriction. When carefully examined under magnification, the iris does not constrict uniformly with attempted near vision. Only the re-innervated segments contract, producing a slightly irregular contour to the pupil. (4) [Denervation supersensitivity]. Like any denervated muscle, the iris becomes supersensitive to its normal neurotransmitter (in this case, acetylcholine). Very weak solutions of cholinergic substances such as pilocarpine (that have no effect on the normal iris) cause the denervated iris to constrict. Tonic pupils are usually due to Adie syndrome, but other diseases can denervate the ciliary ganglion. Peripheral neuropathies (such as diabetic neuropathy) occasionally produce tonic pupils. Herpes zoster virus can attack the ciliary ganglion. Trauma to the orbit can damage the short ciliary nerves. Anything that denervates the ciliary ganglion will produce a tonic pupil due to aberrant nerve regeneration. Adie syndrome[SUP][/SUP]is tonic pupil plus absent deep tendon reflexes. Adie syndrome is a fairly common, benign, idiopathic neuropathy that selectively affects the ciliary ganglion and the spinal cord neurons involved in deep tendon reflex arcs. It usually develops in middle age, although it can occur in children. A variant of Adie syndrome, Ross syndrome, affects sweating as well. Early in the course of Adie syndrome (when the cells of the ciliary ganglion have been destroyed, but before regeneration has occurred) the pupil will be fixed and dilated. The sphincter pupillae will be paralyzed. There will be no response to accommodation ”“ the ciliary muscle is also paralyzed. With aberrant nerve regeneration, the pupil will remain fixed, but it will constrict with attempted near vision. The constriction will be abnormal (“tonic”). Late in the course of Adie syndrome, the pupil becomes small (as all pupils do with old age). It will still be “fixed” (it will not constrict to bright light) and it will continue to show abnormal, tonic constriction with attempted near vision. ************************************************************************ 2) The pterygopalatine ganglion (Syn: ganglion pterygopalatinum, meckel's ganglion, nasal ganglion, sphenopalatine ganglion) is a parasympathetic ganglion found in the pterygopalatine fossa. The flow of blood to the nasal mucosa, in particular the venous plexus of the conchae, is regulated by the pterygopalatine ganglion and heats or cools the air in the nose. The pterygopalatine ganglion (of Meckel), the largest of the parasympathetic ganglia associated with the branches of the Maxillary Nerve, is deeply placed in the pterygopalatine fossa, close to the sphenopalatine foramen. It is triangular or heart-shaped, of a reddish-gray color, and is situated just below the maxillary nerve as it crosses the fossa. The pterygopalatine ganglion supplies the lacrimal gland, paranasal sinuses, glands of the mucosa of the nasal cavity and pharynx, the gingiva, and the mucous membrane and glands of the hard palate. It communicates anteriorly with the nasopalatine nerve. [h=2]Roots[/h] It receives a sensory, a parasympathetic, and a sympathetic root. [h=3]Sensory root[/h] Its sensory root is derived from two sphenopalatine branches of the maxillary nerve; their fibers, for the most part, pass directly into the palatine nerves; a few, however, enter the ganglion, constituting its sensory root. [h=3]Parasympathetic root[/h] Its parasympathetic root is derived from the nervus intermedius (a part of the facial nerve) through the greater petrosal nerve. In the pterygopalatine ganglion, the preganglionic parasympathetic fibers from the greater petrosal branch of the facial nerve synapse with neurons whose postganglionic axons, vasodilator, and secretory fibers are distributed with the deep branches of the trigeminal nerve to the mucous membrane of the nose, soft palate, tonsils, uvula, roof of the mouth, upper lip and gums, and upper part of the pharynx. It also sends postganglionic parasympathetic fibers to the lacrimal nerve (a branch of the Ophthalmic nerve, also part of the trigeminal nerve) via the zygomatic nerve, a branch of the maxillary nerve (from the trigeminal nerve), which then arrives at the lacrimal gland. The nasal glands are innervated with secretomotor from the nasopalatine and greater palatine nerve. Likewise, the palatine glands are innervated by the nasopalatine, greater palatine nerve and lesser palatine nerves. The pharyngeal nerve innervates pharyngeal glands. These are all branches of maxillary nerve. [h=3]Sympathetic root[/h] The ganglion also consists of sympathetic efferent (postganglionic) fibers from the superior cervical ganglion. These fibers, from the superior cervical ganglion, travel through the carotid plexus, and then through the deep petrosal nerve. The deep petrosal nerve joins with the greater petrosal nerve to form the nerve of the pterygoid canal, which enters the ganglion. [h=3]Branches[/h] Orbital branches? (See "Innervation" section of ethmoid sinus page.) Nasopalatine nerve Greater palatine nerve Lesser palatine nerve Posterior superior nasal branch pharyngeal branch of maxillary nerve ************************************************************************ 3) The submandibular ganglion (or submaxillary ganglion in older texts) is part of the human autonomic nervous system. [h=2]Function[/h] The submandibular ganglion is responsible for innervation of two salivary glands: the submandibular gland and sublingual gland. [h=2]Location and relations[/h] The submandibular ganglion is small and fusiform in shape. It is situated above the deep portion of the submandibular gland, on the hyoglossus muscle, near the posterior border of the mylohyoid muscle. The ganglion 'hangs' by two nerve filaments from the lower border of the lingual nerve (itself a branch of the mandibular nerve, CN V[SUB]3[/SUB]). It is suspended from the lingual nerve by two filaments, one anterior and one posterior. Through the posterior of these it receives a branch from the chorda tympani nerve which runs in the sheath of the lingual nerve. [h=2]Fibers[/h] Like other parasympathetic ganglia of the head and neck, the submandibular ganglion is the site of synapse for parasympathetic fibers and carries other types of nerve fiber that do not synapse in the ganglion. In summary, the fibers carried in the ganglion are: Sympathetic fibers from the external carotid plexus, via the facial nerve and its branches. These do not synapse in this ganglion. Preganglionic parasympathetic fibers from the superior salivatory nucleus of the medulla oblongata, via the chorda tympani and lingual nerve, which synapse at the origin of: Postganglionic parasympathetic fibers to the oral mucosa and the submandibular and sublingual salivary glands.They are secretomotor to these glands. 4) The otic ganglion is a small, oval shaped, flattened parasympathetic ganglion of a reddish-gray color, located immediately below the foramen ovale in the infratemporal fossa. It gives innervation to the parotid gland for salivation. It is occasionally absent Filaments that pass through the ganglion without synapsing: Nerve to tensor tympani (coming from the trigeminal nerve motor nucleus) Nerve to tensor veli palatini (coming from the trigeminal nerve motor nucleus) [h=3]Branches of communication[/h] Its sympathetic postganglionic fibers consists of a filament from the plexus surrounding the middle meningeal artery. Preganglionic parasympathetic fibers originate from the glossopharyngeal nerve via the lesser petrosal nerve. The lesser petrosal nerve is a continuation of the glossopharyngeal nerve after it exits the skull via the jugular foramen and innervates the tympanic plexus. Postganglionic parasympathetic fibers travel with the sympathetic fibers of the auriculotemporal nerve (a branch of CN V3) to supply the parotid gland. All postsynaptic parasympathetics will use some branch of the Trigeminal Nerve to get from one of four parasympatheic ganglia (Otic, Ciliary, Submandibular, and Pteryopalatine) to their destinations in either smooth muscle or glandular tissue (secretomotor). A slender filament (sphenoidal) ascends to the nerve of the Pterygoid canal, and a small branch connects with the chorda tympani. It is connected by two or three short filaments with the nerve to the Pterygoideus internus, from which it may obtain a motor, and possibly a sensory root. [h=3]Distribution[/h] Its branches of distribution are: a filament to the Tensor tympani, and one to the Tensor veli palatini. The former passes backward, lateral to the auditory tube; the latter arises from the ganglion, near the origin of the nerve to the Pterygoideus internus, and is directed forward. The fibers of these nerves are, however, mainly derived from the nerve to the Pterygoideus internus. ********************************************************************
2 more imp Ganglia 2 more imp Ganglia The geniculate ganglion (from Latin genu, for "knee"[SUP][1][/SUP]) is an L-shaped collection of fibers and sensory neurons of the facial nerve located in the facial canal of the head. It receives fibers from the motor, sensory, and parasympathetic components of the facial nerve and sends fibers that will innervate the lacrimal glands, submandibular glands, sublingual glands, tongue, palate, pharynx, external auditory meatus, stapedius, posterior belly of the digastric muscle, stylohyoid muscle, and muscles of facial expression. The geniculate ganglion contains special sensory neuronal cell bodies for taste, from fibers coming up from the tongue through the chorda tympani and from fibres coming up from the roof of the palate through the greater petrosal nerve (MJ Fitzgerald et al. Clinical Neuroanatomy and Neuroscience). Sensory and parasympathetic inputs are carried into the geniculate ganglion via the nervus intermedius. Motor fibers are carried via the facial nerve proper. The greater petrosal nerve, which carries sensory fibers as well as preganglionic parasympathetic fibers, emerges from the anterior aspect of the ganglion. The geniculate ganglion is one of several ganglia of the head and neck. Like the others, it is a bilaterally distributed structure, with each side of the face having a geniculate ganglion. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx The trigeminal ganglion (or Gasserian ganglion, or semilunar ganglion, or Gasser's ganglion) is a sensory ganglion of the trigeminal nerve (CN V) that occupies a cavity (Meckel's cave) in the dura mater, covering the trigeminal impression near the apex of the petrous part of the temporal bone. Relations It is somewhat crescentic in shape, with its convexity directed forward: Medially, it is in relation with the internal carotid artery and the posterior part of the cavernous sinus. The motor root runs in front of and medial to the sensory root, and passes beneath the ganglion; it leaves the skull through the foramen ovale, and, immediately below this foramen, joins the mandibular nerve. The greater superficial petrosal nerve lies also underneath the ganglion. The ganglion receives, on its medial side, filaments from the carotid plexus of the sympathetic. It gives off minute branches to the tentorium cerebelli, and to the dura mater in the middle fossa of the cranium. From its convex border, which is directed forward and lateralward, three large nerves proceed, viz., the ophthalmic (V[SUB]1[/SUB]), maxillary (V[SUB]2[/SUB]), and mandibular (V[SUB]3[/SUB]). The ophthalmic and maxillary consist exclusively of sensory fibers; the mandibular is joined outside the cranium by the motor root. Clinical significance After recovery from a primary herpes infection, the virus is not cleared from the body, but rather lies dormant in a non-replicating state within the trigeminal ganglion. Herpes Labialis may follow from primary herpes infection/herpetic gingivostomatitis The trigeminal ganglion is damaged, by infection or surgery, in trigeminal trophic syndrome. Trigeminal trophic syndrome causes paresthesias and anesthesia, which may lead to erosions of the nasal ala. The thermocoagulation or injection of glycerol into the trigeminal ganglion has been used in the treatment of trigeminal neuralgia. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx (-:
3 imp. conditions / diseases of the pupil 3 imp. conditions / diseases of the pupil Argyll Robertson pupils (“AR pupils” or "Prostitute's Pupil") are bilateral small pupils that constrict when the patient focuses on a near object (they “accommodate”), but do not constrict when exposed to bright light (they do not “react” to light). They are a highly specific sign of neurosyphilis. In general, pupils that “accommodate but do not react” are said to show light-near dissociation. A video of AR pupils and light-near dissociation is available here AR pupils are extremely uncommon in the developed world. There is continued interest in the underlying pathophysiology, but the scarcity of cases makes ongoing research difficult. Pathophysiology The two different types of near response are caused by different underlying disease processes. Adie's pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision). The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear. Studies have failed to demonstrate a focal localising lesion. Research has implicated the rostral mid-brain in the vicinity of the cerebral aqueduct of the third ventricle as the most likely region of damage. A lesion in this area would involve efferent pupillary fibres on the dorsal aspect of the Edinger-Westphal nucleus (associated with the response to light) while sparing the fibres associated with the response to near, which lie slightly more ventrally.[SUP][3][/SUP] The exact relationship between syphilis and the two types of pupils (AR pupils and tonic pupils) is not known at the present time. The older literature on AR pupils did not report the details of pupillary constriction (brisk vs. tonic) that are necessary to distinguish AR pupils from tonic pupils. Tonic pupils can occur in neurosyphilis.[SUP][4][/SUP] It is not known whether neurosyphilis itself (infection by Treponema pallidum) can cause tonic pupils, or whether tonic pupils in syphilis simply reflect a coexisting peripheral neuropathy. Thompson and Kardon (2006) summarize the present view: The evidence supports a midbrain cause of the AR pupil, provided one follows Loewenfeld’s definition of the AR pupil as small pupils that react very poorly to light and yet seem to retain a normal pupillary near response that is definitely not tonic.To settle the question of whether the AR pupil is of central or peripheral origin, it will be necessary to perform iris transillumination (or a magnified slit-lamp examination) in a substantial number of patients who have a pupillary light-near dissociation (with and without tonicity of the near reaction), perhaps in many parts of the world. xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Parinaud's Syndrome, also known as dorsal midbrain syndrome is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology. cross section of midbrain showing lesion Signs and symptoms Parinaud's Syndrome is a cluster of abnormalities of eye movement and pupil dysfunction, characterized by: Paralysis of upgaze: Downward gaze is usually preserved. This vertical palsy is supranuclear, so doll's head maneuver should elevate the eyes, but eventually all upward gaze mechanisms fail. Pseudo-Argyll Robertson pupils: Accommodative paresis ensues, and pupils become mid-dilated and show light-near dissociation. Convergence-Retraction nystagmus: Attempts at upward gaze often produce this phenomenon. On fast up-gaze, the eyes pull in and the globes retract. The easiest way to bring out this reaction is to ask the patient to follow down-going stripes on an optokinetic drum. Eyelid retraction (Collier's sign) Conjugate down gaze in the primary position: "setting-sun sign". Neurosurgeons will often see this sign most commonly in patients with failed ventriculoperitoneal shunts. It is also commonly associated with bilateral papilledema. It has less commonly been associated with spasm of accommodation on attempted upward gaze, pseudoabducens palsy (also known as thalamic esotropia) or slower movements of the abducting eye than the adducting eye during horizontal saccades, see-saw nystagmus and associated ocular motility deficits including skew deviation, oculomotor nerve palsy, trochlear nerve palsy and internuclear ophthalmoplegia. Causes Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye. Classically, it has been associated with three major groups: Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome. Women in their 20s-30s with multiple sclerosis Older patients following stroke of the upper brainstem However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome. Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose. Prognosis and Treatment The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3-6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported. Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well. ***************************************************************** Marcus Gunn pupil or relative afferent pupillary defect (RAPD) is a medical sign observed during the swinging-flashlight test[SUP][1][/SUP] whereupon the patient's pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced. The most common cause of Marcus Gunn pupil is a lesion of the optic nerve (between the retina and the optic chiasm) or severe retinal disease. It is named after Scottish ophthalmologist Robert Marcus Gunn. Examination The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye. In the swinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at. This indicates an intact direct and consensual pupillary light reflex. When the test is performed in an eye with an afferent pupillary defect, light directed in the affected eye will cause only mild constriction of both pupils (due to decreased response to light from the afferent defect), while light in the unaffected eye will cause a normal constriction of both pupils (due to an intact afferent path, and an intact consensual pupillary reflex). Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye. A Marcus Gunn Pupil is distinguished from a total CN II lesion, in which the affected eye perceives no light. In that case, shining the light in the affected eye produces no effect. Anisocoria is absent. A Marcus Gunn pupil is seen, among other conditions, in optic neuritis. It is also common in retrobulbar optic neuritis due to multiple sclerosis but only for 3-4 weeks, until the visual acuity begins to improve in 1–2weeks and may return to normal. (-:
Cranial Nerve 4 in focus I have put together some matter on Cranial Nerve 4 ( drawn mainly from Gray's and Snell's Neuroanatomy ) Isolated injury to the fourth nerve can be caused by any process that stretches or compresses the nerve. Even relatively minor trauma can transiently stretch the fourth nerve (by transiently displacing the brainstem relative to the posterior clinoid process). Patients with minor damage to the fourth nerve will complain of “blurry” vision. Patients with more extensive damage will notice frank diplopia and rotational (torsional) disturbances of the visual fields. The usual clinical course is complete recovery within weeks to months. A generalized increase in intracranial pressure ”“ hydrocephalus, pseudotumor cerebri, hemorrhage, edema ”“ will affect the fourth nerve, but the abducens nerve (VI) is usually affected first (producing horizontal diplopia, not vertical diplopia). Infections (meningitis, herpes zoster), demyelination (multiple sclerosis), diabetic neuropathy and cavernous sinus disease can affect the fourth nerve, as can orbital tumors and Tolosa-Hunt syndrome. In general, these diseases affect other cranial nerves as well. Isolated damage to the fourth nerve is uncommon in these settings. Injury to the trochlear nerve cause weakness of downward eye movement with consequent vertical diplopia (double vision). The affected eye drifts upward relative to the normal eye, due to the unopposed actions of the remaining extraocular muscles. The patient sees two visual fields (one from each eye), separated vertically. To compensate for this, patients learn to tilt the head forward (tuck the chin in) in order to bring the fields back together ”“ to fuse the two images into a single visual field. This accounts for the “dejected” appearance of patients with “pathetic nerve” palsies. As would be expected, the diplopia gets worse when the affected eye looks toward the nose ”“ the contribution of the superior oblique muscle to downward gaze is greater in this position. Common activities requiring this type of convergent gaze are reading the newspaper and walking down stairs. Diplopia associated with these activities may be the initial symptom of a fourth nerve palsy. The trochlear nerve is unique among the cranial nerves in several respects. 1) It is the smallest nerve in terms of the number of axons it contains. 2) It has the greatest intracranial length. 3) Other than the optic nerve (cranial nerve II), it is the only cranial nerve that decussates (crosses to the other side) before innervating its target. 4) Finally, it is the only cranial nerve that exits from the dorsal aspect of the brainstem. (-:
Some closely related neuro-opthalmic conditions A cluster of diseases related to the orbit ( i.e sup. orbital fissure syndrome, orbital apex syndrome, cavernous sinus syndrome & orbital cellulitis ) are a constant cause of confusion, because the patient profile and presentation is very similar for the most part. Questions on these topics can feature in ENT, Opthalm, Surgery or Critical Care sections and if you are not sure of the subtle differences that differentiate them you may get all of them wrong I have made an attempt to demystify these and other closely related conditions such as: preseptal cellulitis (aka periorbital cellulitis), Subperiosteal abscess, Orbital abscess and Rhino-orbital mucormycosis. [TABLE="class: LightShading-Accent11"] [TR] [TD] Features[/TD] [TD] Sup Orb Fissure Synd aka Rochon-Duvigneaud's syndrome[/TD] [TD="width: 312"] Orbital Apex Synd aka Jacod syndrome aka post. orbital cellulitis[/TD] [TD="width: 340"] Cavernous Sinus Syndrome[/TD] [TD="width: 266"] Orbital Cellulitis[/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] Source[/TD] [TD="width: 378"] fracture, ethmoid sinusitis[/TD] [TD="width: 312"] posterior ethmoid or sphenoid sinus Rhinocerebral mucormycosis in patients with diabetes mellitus is the most frequent cause of orbital apex syndrome. may be caused by a tumor of the middle cranial fossa (near the apex of the orbit) and by herpes zoster.[/TD] [TD="width: 340"] Nose(dangerous area of face), sinuses, orbit, ear, pharynx, sella turcica (due to mass effect of sella turcica tumor) CST most commonly results from contiguous spread of infection from the nasal furuncle (50%), sphenoidal or ethmoidal sinuses (30%) and dental infections (10%) – Merck manual Communications of cavernous sinus and sources of infection 1. Anteriorly, the superior and inferior ophthalmic veins drain in the sinus. These veins receive blood from face, nose, paranasal sinuses and orbits, Therefore, infection to cavernous sinus may spread from infected facial wounds, eryseplas, squeezing of stye, furuncles, orbital cellulitis and sinusitis. 2. Posteriorly, the superior and inferior petrosal sinuses leave it to join the lateral sinus. Labyrinthine veins opening into the inferior petrosal sinuses bring infections from the middle ear. Mastoid emissary veins may spread infection from the mastoid air cells. 3. Superiorly, the cavernous sinus communicates with veins of the cerebrum and may be infected from meningitis and cerebral abscesses. 4. Inferiorly, the sinus communicates with pterygoid venous plexus. 5. Medially, the two cavernous sinuses are connected with each other by transverse sinuses which account for transfer of infection from one side to the other. [/TD] [TD="width: 266"] Sinus-related, most commonly ethmoidal, typically affects children and young adults Extension of preseptal cellulitis through the orbital septum Local spread from adjacent dacryocystitis, mid-facial or dental infection. The last condition may cause orbital cellulitis via an intermediary maxillary sinusitis. Post-traumatic develops within 72 hours of an injury that penetrates the orbital septum. The typical clinical features may be masked by associated laceration or haematoma.[/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] Onset [/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"] Abrupt with high fever and chills with near signs of toxaemia. Oedema of eyelids, chemosis and proptosis [/TD] [TD="width: 266"] comparitively Slow (wrt css); starts with oedema of eyelids the inner canthus → chemosis → proptosis [/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] Signs and Symp [/TD] [TD="width: 378"] [FONT=&] diplopia[/FONT][FONT=&], [/FONT][FONT=&]paralysis[/FONT][FONT=&] of extraocular motions, [/FONT][FONT=&]exophthalmos[/FONT][FONT=&], [/FONT][FONT=&]ptosis[/FONT][FONT=&] and loss/impaired of sensation along [/FONT][FONT=&]V[SUB]1[/SUB][/FONT] [/TD] [TD="width: 312"] complete ophthalmoplegia, ptosis, decreased corneal sensation, and vision loss The most common finding is oculomotor nerve dysfunction leading to ophthalmoplegia. This is often accompanied by ophthalmic nerve dysfunction, leading to hypoesthesia of the upper face. The optic nerve may eventually be involved, with resulting visual impairment. Unlike cavernous sinus thrombosis, the vision loss is present early. Patients usually develop optic nerve signs, such as a relative afferent pupillary defect. [/TD] [TD="width: 340"] Classic presentations are abrupt onset of unilateral periorbital edema, headache (Severe pain in the eye and forehead on the affected side), vomiting, photophobia, and bulging of the eye (proptosis) in a seriously ill patient having high grade fever with rigors Papilledema, retinal hemorrhages, and decreased visual acuity and blindness may occur from venous congestion within the retina Conjunctiva is swollen and congested. Headache with nuchal rigidity may occur. Pupil may be dilated and sluggishly reactive. Infection can spread to contralateral cavernous sinus within 24–48 hours of initial presentation. Oedema in mastoid region is a pathognomonic sign. It is due to back pressure in the mastoid emissary vein. [/TD] [TD="width: 266"] Presentation is with the rapid onset of severe malaise, fever, pain and visual impairment Unilateral tender warm and red periorbital and lid oedema. Painful ophthalmoplegia. Proptosis, often obscured by lid swelling, is most frequently lateral and downwards. [/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] CN involvm.[/TD] [TD="width: 378"] [FONT=&] superior and inferior divisions of [/FONT][FONT=&]oculomotor nerve[/FONT][FONT=&] (III) [/FONT] [FONT=&]trochlear nerve[/FONT][FONT=&] (IV) [/FONT] [FONT=&]lacrimal[/FONT][FONT=&], [/FONT][FONT=&]frontal[/FONT][FONT=&] and [/FONT][FONT=&]nasociliary[/FONT][FONT=&] branches of [/FONT][FONT=&]ophthalmic nerve[/FONT][FONT=&] ([/FONT][FONT=&]V[SUB]1[/SUB][/FONT][FONT=&]) [/FONT] [FONT=&]abducens nerve[/FONT][FONT=&] (VI)[/FONT][/TD] [TD="width: 312"] [FONT=&] superior and inferior divisions of [/FONT][FONT=&]oculomotor nerve[/FONT][FONT=&] (III) [/FONT] [FONT=&]trochlear nerve[/FONT][FONT=&] (IV) [/FONT] [FONT=&]lacrimal[/FONT][FONT=&], [/FONT][FONT=&]frontal[/FONT][FONT=&] and [/FONT][FONT=&]nasociliary[/FONT][FONT=&] branches of [/FONT][FONT=&]ophthalmic nerve[/FONT][FONT=&] ([/FONT][FONT=&]V[SUB]1[/SUB][/FONT][FONT=&]) [/FONT] [FONT=&]abducens nerve[/FONT][FONT=&] (VI)[/FONT] [FONT=&]+[/FONT] [FONT=&]Optic nerve involvement[/FONT] [FONT=&]Typical[/FONT][FONT=&]triad of:[/FONT] [FONT=&](i) ophthalmoplegia due to paresis of third, fourth and sixth cranial nerves; [/FONT] [FONT=&](ii) anaesthesia in the region of supply of ophthalmic division of fifth nerve; and [/FONT] [FONT=&](iii) amaurosis due to involvement of optic nerve.[/FONT][/TD] [TD="width: 340"] CN involvement similar to Sup orb apex synd + added involvement of V2(maxillary branch of trigeminal) [FONT=&]Involvement vertically, from superior to inferior (within the lateral wall of the sinus) in this order (Involved individually and sequentially)[/FONT] [FONT=&]oculomotor nerve[/FONT][FONT=&] (CN III)[/FONT] [FONT=&]trochlear nerve[/FONT][FONT=&] (CN IV)[/FONT] [FONT=&]abducens nerve[/FONT][FONT=&] (CN VI)[/FONT] [FONT=&]ophthalmic nerve[/FONT][FONT=&], the V[SUB]1[/SUB] branch of the [/FONT][FONT=&]trigeminal nerve[/FONT][FONT=&] (CN V)[/FONT] [FONT=&]maxillary nerve[/FONT][FONT=&], the V[SUB]2[/SUB] branch of CN V[/FONT] Horner's syndrome can also occur due to involvement of the carotid ocular sympathetics, but may be difficult to appreciate in the setting of a complete third nerve injury[/TD] [TD="width: 266"] all concerned cranial nerves Involved concurrently with complete ophthalmoplegia[/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] Other structures (directly involved)[/TD] [TD="width: 378"][FONT=&] superior and inferior divisions of [/FONT][FONT=&]ophthalmic vein[/FONT][FONT=&]. [/FONT] [FONT=&] Inferior division also passes through the [/FONT][FONT=&]inferior orbital fissure[/FONT][FONT=&]. [/FONT] [FONT=&]sympathetic fibers[/FONT][FONT=&] from [/FONT][FONT=&]cavernous plexus[/FONT][/TD] [TD="width: 312"][/TD] [TD="width: 340"] internal carotid artery[/TD] [TD="width: 266"] Orbital wall, eyelids + all structures within the orbit[/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] Laterality[/TD] [TD="width: 378"] Unilateral[/TD] [TD="width: 312"] Unilateral[/TD] [TD="width: 340"] Bilaterality is common[/TD] [TD="width: 266"] Unilateral[/TD] [/TR] [TR] [TD="width: 108"][/TD] [TD="width: 378"][/TD] [TD="width: 312"][/TD] [TD="width: 340"][/TD] [TD="width: 266"][/TD] [/TR] [TR] [TD="width: 108"] Extra Edge[/TD] [TD="width: 1296, colspan: 4"] Orbital apex, Superior orbital fissure and cavernous sinus, are anatomically close to each other so that syndromes have been used to describe the anatomical locations of a disease process. However the etiology, diagnostic evaluation and management are similar for each of these conditions. Among all these presentations taken together Cavernous sinus syndrome is the most common and orbital apex syndrome is the least. Patients may have both Superior orbital fissure + Orbital apex syndrome. Typically, if blindness is present with superior orbital syndrome, it is called orbital apex syndrome. The nerves passing through the fissure can be remembered with the mnemonic, "Live Frankly To See Absolutely No Insult" - for Lacrimal, Frontal, Trochlear, Superior Division of Oculomotor, Abducens, Nasociliary and Inferior Division of Oculomotor nerve Orbital cellulitisrefers to an acute infection of the soft tissues of the orbit behind the orbital septum. Orbital cellulitis may or may not progress to a subperiosteal abscess or orbital abscess In orbital cellulitis, signs of marked orbital inflammation usually precede visual loss. In orbital apex syndrome (“posterior orbital cellulitis”), the opposite occurs. Patients present with severe unilateral visual loss and ophthalmoplegia, but with minimal orbital inflammation. Staphylococcus aureus is the most common infectious microbe, found in 70% of the cases. Streptococcus is the second leading cause. In preseptal cellulitis (aka periorbital cellulitis), in contrast to orbital cellulitis proptosis and chemosis are absent; visual acuity, pupillary reactions and ocular motility are unimpaired. (Preseptal cellulitis is an infection of the subcutaneous tissues anterior to the orbital septum.) Modes of intection 1. Exogenous infection may result following skin laceration or insect bites. 2. Extension from local infections such as from an acute hordeolum or acute dacryocystitis. 3. Endogenous infection may occur by haematogenous spread from remote infection of the middle ear or upper respiratory tract. Subperiosteal abscessis collection of purulent material between the orbital bony wall and periosteum, most frequently located along the medial orbital wall. Clinically, subperiosteal abscess is suspected when clinical features of orbital cellulitis are associated with eccentric proptosis(as opposed to axial proptosis in case of orbital cellulitis); but the diagnosis is confirmed by CT scan Orbital abscessis collection of pus within the orbital soft tissue. Clinically it is suspected by signs of severe proptosis, marked chemosis, complete ophthalmoplegia, and pus points below the conjunctiva, but is confirmed by CT scan. Rhino-orbital mucormycosis Mucormycosis is a very rare opportunistic infection caused by fungi of the family Mucoraceae, which typically affects patients with diabetic ketoacidosis or immunosuppression. This aggressive and often fatal infection is acquired by the inhalation of spores, which give rise to an upper respiratory infection. The infection then spreads to the contiguous sinuses and subsequently to the orbit and brain. Invasion of blood vessels by the hyphae results in occlusive vasculitis with ischaemic infarction of orbital tissues. A necrotizing reaction destroys muscles,nbone and soft tissue, frequently without causing signs of orbital cellulitis. Presentation is with gradual onset facial and periorbital swelling, diplopia and visual loss. Progression is slower than in bacterial orbital cellulitis. Complications include retinal vascular occlusion, multiple cranial nerve palsies and cerebrovascular occlusion. If not treated energetically, patient develops meningitis, brain abscess and dies within days to weeks. Diagnosis is made clinically and confirmed by biopsy of the involved area and finding of nonseptate broad branching hyphae. Investigations, where appropriate, include the following: • White cell count. • Blood culture. • X-ray PNS to identify associated sinusitis. • Orbital ultrasonography to detect intra-orbital abscess. • CT of the orbit, sinuses and brain. CT scan and MRI are useful: Ã in differentiating between preseptal and postseptal cellulitis; Ã in detecting subperiosteal abscesses and orbital abscesses. Ã in detecting intracranial extension; Ã in deciding when and from where to drain an orbital abscess. • Lumbar puncture if meningeal or cerebral signs develop. Treatment •Intravenous antifungal agents such as amphotericin. •Daily packing and irrigation of the involved areas with amphotericin. •Wide excision of devitalized and necrotic tissues. •Adjunctive hyperbaric oxygen may be helpful. •Correction of the underlying metabolic defect, if possible. •Exenteration may be required in unresponsive cases. V Imp Note Antibiotic therapy in very serious infections involvesintravenous ceftazidime/nafcicillin, with oral metronidazole to cover anaerobes. Vancomycin is a useful alternative in the context of penicillin allergy. Antibiotic therapy should be continued until the patient has been apyrexial for 4 days. Once culture sensitivity results are available shift to the specific antibiotic and Surgical intervention in which the infected sinuses and orbital collections are drained should be considered in the following circumstances: • Lack of response to antibiotics. (Monitoring of optic nerve function every 4 hours by testing pupillary reactions, visual acuity, colour vision and light brightness appreciation.) • Subperiosteal or intracranial abscess. • Atypical picture, which may merit a biopsy. Caution 1)Post-traumatic orbital cellulitis develops within 72 hours of an injury that penetrates the orbital septum. The typical clinical features may be masked by associated laceration or haematoma. 2) When you encounter a lid swelling in the setting of a PNS infection, check if it is inflamed. If it is,then it it could be something more sinister (orbital cellulitis or preseptal cellulitis) than a harmless reactive swelling. Don’t feel shy to ask for an opthalmologic consultation 3) Orbital apex syndrome(according to ENT textbook by Dhingra). It is superior orbital fissure syndrome with additional involvement of the optic nerve and maxillary division of the trigeminal (V[SUB]2[/SUB])Ã wrong, see above. [/TD] [/TR] [/TABLE] (-:
Some images to further consolidate the identification of the different closely related conditions in the above post
UMN vs LMN lesion of tongue First up a scenario involving LMN lesion of tongue musculature [FONT=&]A patient displays a deviation of the tongue to the left and a hemiparesis on the right side. The lesion is located in which of the following regions?[/FONT] [FONT=&]A. Right hypoglossal nucleus[/FONT] [FONT=&]B. Left hypoglossal nucleus[/FONT] [FONT=&]C. Right inferior frontal lobe[/FONT] [FONT=&]D. Right ventromedial medulla[/FONT] [FONT=&]E. Left ventromedial medulla [/FONT][FONT=&]EXPLANATION: A lesion of the left ventromedial medulla would produce a disorder referred to as "alternating hypoglossal hemiplegia" in which there is damage to the hypoglossal nerve as it is about to exit the brainstem and to the pyramidal tract. Damage to the hypoglossal nerve causes a deviation of the tongue to the side of the lesion when it is protruded and a contralateral UMN paralysis of the limbs because these descending corticospinal fibers cross at the medulla-spinal cord border. The other choices do not include structures that were affected in this case. The choice involving the right ventromedial medulla is incorrect because the tongue deviated to the left, not the right side and the paralysis was on the right side of the body, not the left.[/FONT] [FONT=&]The answer is E. [/FONT] [h=2]UMN lesion involving the tongue[/h] [FONT=&]A 76-year-old woman who has a 10-year history of high blood pressure and diabetes was reaching for a jar of flour to make an apple pie, when her right side suddenly gave out, and she collapsed. While trying to get up from the floor, she noticed that she was unable to move her right arm or leg. She attempted to cry for help because she was unable to reach the telephone; however, her speech was slurred and rather unintelligible. She lay on the floor and waited for help to arrive. Her son began to worry about his usually prompt mother when she did not arrive with her apple pie. After several attempts to telephone her apartment without getting an answer, he drove there and found her lying on the floor. She attempted to tell him what had happened, but her speech was too slurred to comprehend. Assuming that his mother had had a stroke, the son called an ambulance. A neurology resident was called to see the patient in the emergency room because the physicians there likewise thought that she had a stroke. The resident noted that she followed commands very well, and, although her speech was very slurred, it was logical in organization. The lower two-thirds of her face drooped on the right. Her tongue pointed to the right side when she was asked to protrude it. Her right arm and leg were severely, but equally, weak; her left side had normal strength. She felt a pin and a vibrating tuning fork equally on both sides. Where in the central nervous system (CNS) did her stroke most likely occur?[/FONT] [FONT=&]A. Left precentral gyrus[/FONT] [FONT=&]B. Right precentral gyrus[/FONT] [FONT=&]C. Left basilar pons or left internal capsule[/FONT] [FONT=&]D. Right putamen or globus pallidus[/FONT] [FONT=&]E. Left thalamus[/FONT] [FONT=&]EXPLANATION: A CT scan of the patient's head was done in the emergency room, which showed a new infarct or stroke in the genu and anterior portion of the posterior limb of the left internal capsule. This is the region of the internal capsule through which most of the fibers of the corticospinal and corticobulbar tracts pass in a somatotopically organized fashion before entering the brain stem. Because most of these fibers pass through a very small region, a small infarct can cause deficits in a wide distribution of areas. In this case, the patient had weakness in her face and tongue, causing her slurred speech, in addition to weakness of her arm and leg. Since somatosensory fibers destined for the postcentral gyrus occupy a position in the internal capsule caudal to the corticospinal tract fibers, these fibers were spared and she had no sensory deficits. The only other area in the CNS that can cause a pure motor hemiparesis is the basilar pons, an area through which corticospinal and corticobulbar fibers also run. The vascular supply of this region consists of perforators from the basilar artery, which are small and subject to atherosclerotic disease. [/FONT] [FONT=&]The answer is C. Comments - 1) This case is typical of UMN type of lesion in which the tongue is involved. The tongue deviates to the side opposite to that of the lesion as opposed to a LMN lesion in which the tongue deviates to the side of the lesion. 2) Second point as to why this case is imp. Just imagine a lesion affecting the entire precentral gyrus on one side ( middle cerebral artery region ). Can this patient actually be conscious, following such a massive fire selectively involve the precentral gyrus and shy away from the somatosensory area, just next door ? I guess not. And that limit's the possibility of the stoke to the basement area of the brain, where the wires are closely crowded and a small spark can involve large areas ( selectively ). Note : I am not trying to compare the basement area of the brain to a building basement where a small spark can actually gut the entire building. [/FONT]):[FONT=&] [/FONT] [FONT=&]How tongue deviation in Genioglossus palsy is similar to the bending of a bimetallic strip. I have tried to compare the mechanism of deviation to that of a bimetallic strip (the principle behind the thermostat ) . The explanation in the image below says it all....so I am not saying anything further. I have a background in physics from where i get the inspiration to compare aspects of human mechanism and behavior with the physical world and viceversa as well ( since I am a keen observer of human behavior as well (-: ) [/FONT]
Significance of the Lenticulo-striate and anterior choroidal arteries The signficance [FONT=&]The internal capsule is supplied primarily by the lenticulostriate branches of the middle cerebral artery. In addition, portions of the posterior limb of the internal capsule are supplied by the anterior choroidal artery, a branch of the internal carotid artery. Both the lateral striate branches and the anterior choroidal artery are small branches of larger arteries and are more susceptible to damage (atherosclerosis) from high blood pressure and diabetes than the larger vessels. The posterior cerebral artery supplies mainly the occipital lobe and parts of the midbrain; the anterior cerebral artery supplies mainly the medial aspect of the frontal and parietal lobes; the vertebral artery supplies the lower brainstem; and the posterior choroidal artery supplies the medial and superior surfaces of the thalamus, choroid plexus of the third ventricle, and parts of the tectum.[/FONT] A case scenario ( very special case ) [FONT=&]A patient was diagnosed with having a brain infarct and presented primarily with contralateral hemiparesis and dysarthria. Which of the following regions were affected by the infarct? [/FONT] [FONT=&]A. Medial thalamic nuclei[/FONT] [FONT=&]B. Lateral thalamic nuclei[/FONT] [FONT=&]C. Dorsomedial thalamus[/FONT] [FONT=&]D. Ventromedial thalamus[/FONT] [FONT=&]E. Medial hypothalamus[/FONT] [FONT=&]EXPLANATION: [/FONT] [FONT=&]The lateral region of thalamus as well as the posterior limb of internal capsule are supplied by choroidal branches of the internal carotid artery.[/FONT][FONT=&] Infarct of this artery most frequently results in contralateral hemiparesis and dysarthria. Although lesions associated with this artery may affect only motor functions, they may also cause loss of pain, touch, and sometimes visual functions. The other choices given in this question are not associated with this constellation of deficits.[/FONT] [FONT=&]The answer is B.[/FONT] (-:
Dejerine”“Roussy syndrome Dejerine”“Roussy syndrome or thalamic pain syndrome is a condition developed after a thalamic stroke, a stroke causing damage to the thalamus. [h=2]Eponym[/h] Dejerine”“Roussy syndrome has also been referred to as: "Posterior Thalamic Syndrome", "Retrolenticular Syndrome", "Thalamic Hyperesthetic Anesthesia", "Thalamic Pain Syndrome", "Thalamic Syndrome", "Central Pain Syndrome", and "Central Post-Stroke Syndrome".[SUP][/SUP][SUP][/SUP][SUP][/SUP]This condition is not associated with Roussy”“Lévy syndrome or Dejerine”“Sottas disease, both of which are genetic disorders. [SUP][/SUP] [h=2]Symptoms[/h] Dejerine”“Roussy syndrome is most commonly preceded by numbness in the affected side. In these cases, numbness is replaced by burning and tingling sensations, widely varying in degree of severity across all cases.[SUP][/SUP] The majority of those reported are cases in which the symptoms are severe and debilitating.[SUP][/SUP]Burning and tingling can also be accompanied by hypersensitivity, usually in the form of dysaesthesia or allodynia. Less commonly, some patients develop severe ongoing pain with little or no stimuli.[SUP][/SUP] Allodynia refers to hypersensitivity to sensations associated with a stimulus that would normally not cause pain.[SUP][/SUP][SUP][/SUP][SUP][/SUP]For example, there is a patient who experiences unrelenting pain when a breeze touches his skin. Most patients experiencing allodynia, experience pain with touch and pressure, however some can be hypersensitive to temperature.[SUP][/SUP] Dysaesthesia is defined as pain due to thalamic lesioning. This form of neuropathic pain can be any combination of itching, tingling, burning, or searing experienced spontaneously or from stimuli.[SUP][/SUP] Allodynia and dysaesthesia replace numbness between one week and a few months after a thalamic stroke. In general, once the development of pain has stopped, the type and severity of pain will be unchanging and if untreated, persist throughout life. Consequentially, many will undergo some form of pain treatment and adjust to their new lives as best they can. Pain associated with Dejerine”“Roussy syndrome is sometimes coupled with anosognosia or somatoparaphrenia which causes a patient having undergone a right-parietal, or right-sided stroke to deny any paralysis of the left side when indeed there is, or deny the paralyzed limb(s) belong to them.[SUP][/SUP] Although debatable, these symptoms are rare and considered part of a "thalamic phenomenon", and are not normally considered a characteristic of Dejerine”“Roussy syndrome. [h=3]Proposed mechanism[/h] The imbalance in sensation characterized by Dejerine”“Roussy syndrome can be argued through a model addressing a system of inputs and outputs that the brain must constantly process throughout life, suggesting latent plasticity. The right and left hemispheres of the brain both play important roles in the sensory input and output.[SUP][/SUP] When a stroke damages one hemisphere, it is proposed that the other hemisphere will cope with the discrepancies in a specific manner. The left hemisphere tends to "gloss over" discrepancies from inputs, eliciting either denial or rationalization defense mechanisms in order to stabilize said discrepancy. In contrast, the right hemisphere does the opposite, and will focus on the discrepancy, and motivate action to be taken to restore equilibrium. Therefore, damage to the left hemisphere can cause both an indifference to pain and hypersensitivity to pain (dysaesthesia or alloydnia), while damage to the right hemisphere can cause denial as a defense mechanism (anosognosia and somatoparaphrenia). The insular cortex, part of the cerebral cortex, is responsible for self-sensation, including the degree of pain perceived by the body, and for self-awareness and defense mechanisms. The insular cortex is often lesioned by a stroke. Particularly, the posterior insula has been mapped to correlate to pain experienced by an individual. In addition, is has been proven that the posterior insula receives a substantial amount of the inputs of the brain, and can be treated with visual, kinesthetic, and auditory inputs. [h=2]Treatments[/h][h=3]Pharmaceutical treatment[/h] Opiates contain the narcotics morphine, codeine, and papaverine which provide pain relief. Opiates activate opiate receptors in the brain which alter the brain's perception of sensory input, alleviating pain and sometimes inducing pleasure for a short time period. When intravenously administered, opiates can relieve neuropathic pain but only for a time between 4 and 24 hours. After this time window, the pain returns and the patient must be treated again.[SUP][/SUP][SUP][/SUP] Although this method of treatment has been proven to reduce pain, the repetitive use of opiates has also been linked to the activation of the brain's reward system and therefore poses a threat of addiction. The potential destruction opiates can cause have drawn many doctors and patients away from their use.[SUP][/SUP] [SUP][/SUP] Anti-depressants are traditionally administered for treatment of mood disorders, also linked to the thalamus, and can be used to treat Dejerine”“Roussy symptoms. Specifically, tricyclic anti-depressants such as amytriptyline and selective serotonin reuptake inhibitors have been used to treat this symptom and they are effective to some degree within a short time window.[SUP][/SUP][SUP][/SUP] [SUP][/SUP] Anti-convulsants reduce neuronal hyperexcitability, effectively targeting Dejerine”“Roussy syndrome. Gabapentin and pregabalin are the most common anti-convulsants. They have significant efficacy in treatment of peripheral and central neuropathic pain. Treatments last 4”“12 hours and in general are well tolerated, and the occurrence of adverse events does not differ significantly across patients. Commonly reported side-effects are dizziness, decreased intellectual performance, somnolence, and nausea.[SUP][/SUP] [SUP][/SUP] Topical treatment such as lidocaine patches can be used to treat pain locally. The chemical is released to the skin to act as a numbing agent that feels cool, then feels warm, much like IcyHot.[SUP][/SUP] [SUP][/SUP] Kampo medicine has been research in a case study to test the efficacy of a medicine called "Sokeikakketsuto decoction" in Dejerine”“Roussy pain symptoms. The patients studied did not respond to anti-depressants and anti-epileptic drugs, and turned to Kampo medicine as a treatment option. Pain experienced by patients significantly decreased and some had improved dysaesthesia. The mechanism of action blocking pain is currently unknown. The effects of this treatment lasted ~10 days, a comparatively longer refractory period than any of the traditional pharmaceutical treatments. [h=3]Stimulation treatments[/h] Electrode stimulation from surgically implanted electrodes has been studied in the past decade in hopes of a permanent pain treatment without refraction. Electric stimulation utilizing implants deliver specific voltages to a specific part of the brain for specific durations. More recently, research is being done in radiation therapy as long term treatment of Dejerine-Roussy syndrome. In general, these studies have concluded initial efficacy in such implants, but pain often re-appears after a year or so. Long-term efficacy of stimulation treatments must be further tested and evaluated.[SUP][/SUP] [SUP][/SUP] Spinal cord stimulation has been studied in the last couple of years. In a long case study, 8 patients were given spinal cord stimulation via insertion of a percutaneous lead at the appropriate level of the cervical or thoracic spine. Between 36 and 149 months after the stimulations, the patients were interviewed. 6 of the 8 had received initial pain relief, and three experienced long-term pain relief. Spinal cord stimulation is cheaper than brain stimulation and less invasive, and is thus a more promising option for pain treatment.[SUP][/SUP] [SUP][/SUP] Expensive and invasive, the above treatments are not guaranteed to work, and are not meeting the needs of patients. There is a need for a new, less expensive, less invasive form of treatment, one of which is postulated below. In 2007, Dr. V. S. Ramachandran and his lab proposed that caloric stimulation might be effective in treating Dejerine”“Roussy syndrome. They hypothesized that if cold water was streamed into the ear down the auditory canal, the symptoms associated with Dejerine”“Roussy syndrome would be alleviated. Ramachandran stated that he had carried out provisional experiments on two patients and believed that their reactions supported his theory. A classic case on this syndrome [FONT="]A 67-year-old man suffers an infarct of the geniculothalamic branch of the posterior cerebral artery. In particular, there is involvement of nuclei of the posterior thalamus. Which of the following is the most likely effect of such an infarct? [/FONT] [FONT="]A. Emotional volatility in response to an innocuous statement[/FONT] [FONT="]B. Short-term memory loss that occurs about 1 week following the infarct[/FONT] [FONT="]C. Long-term memory loss that occurs about 1 month following the infarct[/FONT] [FONT="]D. Severe pain triggered by cutaneous stimuli applied to the patient[/FONT] [FONT="]E. Spastic paralysis of the contralateral limbs[/FONT] [FONT="] [/FONT] [FONT="]EXPLANATION: [/FONT] [FONT="]The infarct caused damage to posterior thalamic nuclei, which may also include VPL and VPM (Dejerine Roussy disease). When these structures are damaged, a disorder referred to as thalamic pain can ensue. In this condition, light cutaneous stimulation is sufficient to produce severe pain. The projections from nuclei situated in this region project principally to the parietal and occipital lobes and play a role in the regulation of pain (although the precise mechanisms remain unknown). The projections to the occipital cortex relate to visual functions of the neurons of the posterior thalamus that are unrelated to pain. The other processes offered as alternate choices have not been shown to be related to functions of the posterior thalamus. [/FONT] [FONT="]The answer is D. [/FONT](Y)
